PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 25395240-3 2015 Previous studies showed that As2O3 can damage the hERG current via disturbing its trafficking to cellular membrane. Arsenic Trioxide 29-34 ETS transcription factor ERG Homo sapiens 50-54 25824027-0 2015 Arsenic trioxide inhibits breast cancer cell growth via microRNA-328/hERG pathway in MCF-7 cells. Arsenic Trioxide 0-16 ETS transcription factor ERG Homo sapiens 69-73 25824027-2 2015 In a previous study by this group, it was shown that As2O3 induces the apoptosis of MCF-7 breast cancer cells through inhibition of the human ether-a-go-go-related gene (hERG) channel. Arsenic Trioxide 53-58 ETS transcription factor ERG Homo sapiens 170-174 25824027-7 2015 Further investigation using western blot analysis and reverse transcription-quantitative polymerase chain reaction revealed that As2O3 downregulated hERG expression via upregulation of miR-328 expression in MCF-7 cells. Arsenic Trioxide 129-134 ETS transcription factor ERG Homo sapiens 149-153 25824027-8 2015 In conclusion, As2O3 was observed to inhibit breast cancer cell growth, at least in part, through the miR-328/hERG pathway. Arsenic Trioxide 15-20 ETS transcription factor ERG Homo sapiens 110-114 25395240-4 2015 Consistent with these findings, in this study, we reported that As2O3 inhibited hERG channel at both protein and mRNA levels and damaged hERG current but did not affect channel kinetics. Arsenic Trioxide 64-69 ETS transcription factor ERG Homo sapiens 80-84 25395240-4 2015 Consistent with these findings, in this study, we reported that As2O3 inhibited hERG channel at both protein and mRNA levels and damaged hERG current but did not affect channel kinetics. Arsenic Trioxide 64-69 ETS transcription factor ERG Homo sapiens 137-141 25395240-5 2015 Further, we demonstrated that As2O3 up-regulated miR-21 and miR-23a expression in hERG-HEK293 cells and neonatal cardiomyocytes. Arsenic Trioxide 30-35 ETS transcription factor ERG Homo sapiens 82-86 25395240-6 2015 In addition, knock-down of miR-21 by its specific antisense molecules AMO-21 was able to rescue Sp1 and hERG inhibition caused by As2O3. Arsenic Trioxide 130-135 ETS transcription factor ERG Homo sapiens 104-108 25395240-8 2015 This finding revealed that regulation of the NF-kappaB-miR-21-Sp1 signalling pathway is a novel mechanism for As2O3-induced hERG inhibition. Arsenic Trioxide 110-115 ETS transcription factor ERG Homo sapiens 124-128 25395240-10 2015 And the hERG channel inhibition induced by As2O3 was rescued after being transfected with AMO-23a, which may be a molecular mechanism for the role of As2O3 in hERG trafficking deficiency. Arsenic Trioxide 43-48 ETS transcription factor ERG Homo sapiens 8-12 25395240-10 2015 And the hERG channel inhibition induced by As2O3 was rescued after being transfected with AMO-23a, which may be a molecular mechanism for the role of As2O3 in hERG trafficking deficiency. Arsenic Trioxide 43-48 ETS transcription factor ERG Homo sapiens 159-163 25395240-10 2015 And the hERG channel inhibition induced by As2O3 was rescued after being transfected with AMO-23a, which may be a molecular mechanism for the role of As2O3 in hERG trafficking deficiency. Arsenic Trioxide 150-155 ETS transcription factor ERG Homo sapiens 8-12 25395240-10 2015 And the hERG channel inhibition induced by As2O3 was rescued after being transfected with AMO-23a, which may be a molecular mechanism for the role of As2O3 in hERG trafficking deficiency. Arsenic Trioxide 150-155 ETS transcription factor ERG Homo sapiens 159-163 25395240-11 2015 In brief, our study revealed that miR-21 and miR-23a are involved in As2O3-induced hERG deficiency at transcriptional and transportational levels. Arsenic Trioxide 69-74 ETS transcription factor ERG Homo sapiens 83-87 25395240-12 2015 This discovery may provide a novel mechanism of As2O3-induced hERG channel deficiency, and these miRNAs may serve as potential therapeutic targets for the handling of As2O3 cardiotoxicity. Arsenic Trioxide 48-53 ETS transcription factor ERG Homo sapiens 62-66 25395240-12 2015 This discovery may provide a novel mechanism of As2O3-induced hERG channel deficiency, and these miRNAs may serve as potential therapeutic targets for the handling of As2O3 cardiotoxicity. Arsenic Trioxide 167-172 ETS transcription factor ERG Homo sapiens 62-66 25355491-3 2015 The present study was designed to determine whether the expression of hERG gene is regulated by miR-133b or miR-34a, thereby contributing to the anti-proliferation effect of arsenic trioxide (ATO) in U251 human glioma cells. Arsenic Trioxide 174-190 ETS transcription factor ERG Homo sapiens 70-74 25355491-3 2015 The present study was designed to determine whether the expression of hERG gene is regulated by miR-133b or miR-34a, thereby contributing to the anti-proliferation effect of arsenic trioxide (ATO) in U251 human glioma cells. Arsenic Trioxide 192-195 ETS transcription factor ERG Homo sapiens 70-74 25355491-9 2015 The transfection of anti-miR-133b oligonucleotide (AMO-133b) remarkably prevented the decrease of hERG protein by 5 muM ATO treatment for 24 h in U251 cells, whereas anti-miR-34a oligonucleotide (AMO-34a) did not exhibit recuperated effect. Arsenic Trioxide 120-123 ETS transcription factor ERG Homo sapiens 98-102 16418337-3 2006 PAT is chemically related to As2O3, which alters cardiac excitability by inhibition of human ether a-go-go related gene (hERG) trafficking and an increase of cardiac calcium currents. Arsenic Trioxide 29-34 ETS transcription factor ERG Homo sapiens 121-125 25107562-0 2014 The rescuable function and mechanism of resveratrol on As2O3-induced hERG K+ channel deficiency. Arsenic Trioxide 55-60 ETS transcription factor ERG Homo sapiens 69-73 25107562-3 2014 Previous studies showed that As2O3 can damage the human ether-a-go-go-related gene (hERG) current via disturbing its trafficking to cellular membrane. Arsenic Trioxide 29-34 ETS transcription factor ERG Homo sapiens 84-88 25107562-8 2014 Further experiments demonstrate that resveratrol relieved As2O3-caused endoplasmic reticulum (ER) stress by restoring the function of hERG-Hsp70/Hsp90 chaperone complexes and downregulating the protein expression of ER chaperone proteins (calnexin and calreticulin) and activating transcription factor 6. Arsenic Trioxide 58-63 ETS transcription factor ERG Homo sapiens 134-138 21097842-3 2011 We have discovered that arsenic trioxide (As(2)O(3)), a very potent antineoplastic compound for the treatment of acute promyelocytic leukemia, is proarrhythmic via two separate mechanisms: a well characterized inhibition of hERG/I(Kr) trafficking and a poorly understood increase of cardiac calcium currents. Arsenic Trioxide 24-40 ETS transcription factor ERG Homo sapiens 224-228 21097842-3 2011 We have discovered that arsenic trioxide (As(2)O(3)), a very potent antineoplastic compound for the treatment of acute promyelocytic leukemia, is proarrhythmic via two separate mechanisms: a well characterized inhibition of hERG/I(Kr) trafficking and a poorly understood increase of cardiac calcium currents. Arsenic Trioxide 42-51 ETS transcription factor ERG Homo sapiens 224-228 23103450-0 2013 Arsenic trioxide-induced hERG K(+) channel deficiency can be rescued by matrine and oxymatrine through up-regulating transcription factor Sp1 expression. Arsenic Trioxide 0-16 ETS transcription factor ERG Homo sapiens 25-29 23103450-4 2013 Arsenic trioxide (As(2)O(3)), which is used to treat acute promyelocytic leukemia, can cause LQTS type 2 (LQT2) by reducing the hERG current through the diversion of hERG trafficking to the cytoplasmic membrane. Arsenic Trioxide 0-16 ETS transcription factor ERG Homo sapiens 128-132 23103450-4 2013 Arsenic trioxide (As(2)O(3)), which is used to treat acute promyelocytic leukemia, can cause LQTS type 2 (LQT2) by reducing the hERG current through the diversion of hERG trafficking to the cytoplasmic membrane. Arsenic Trioxide 0-16 ETS transcription factor ERG Homo sapiens 166-170 15340016-12 2005 We propose that pentamidine, like arsenic trioxide, produces QT prolongation and torsades de pointes in patients by inhibition of hERG trafficking. Arsenic Trioxide 34-50 ETS transcription factor ERG Homo sapiens 130-134 31218953-7 2019 The combination of As2O3 with resveratrol, on the one hand reduced the expression of hERG channels on the membrane, and on the other hand weaken the binding between hERG and integrin beta 1, which may be the main cause of downstream signaling pathways alterations, including the activation of the apoptotic pathway. Arsenic Trioxide 19-24 ETS transcription factor ERG Homo sapiens 85-89 33842551-7 2021 Arsenic trioxide decreased the expression level of ERG, further promoting cell differentiation. Arsenic Trioxide 0-16 ETS transcription factor ERG Homo sapiens 51-54 31218953-7 2019 The combination of As2O3 with resveratrol, on the one hand reduced the expression of hERG channels on the membrane, and on the other hand weaken the binding between hERG and integrin beta 1, which may be the main cause of downstream signaling pathways alterations, including the activation of the apoptotic pathway. Arsenic Trioxide 19-24 ETS transcription factor ERG Homo sapiens 165-169 31218953-8 2019 CONCLUSION: Taken together, hERG, as a subunit of potassium ion channel on the cell membrane, is highly likely to be involved in the As2O3 and resveratrol induced intracellular signaling cascade disorder, and this novel signaling pathway that sustains the progression of colon cancer may be a promising therapeutic target for human colon cancer treatment in the future. Arsenic Trioxide 133-138 ETS transcription factor ERG Homo sapiens 28-32 30127993-6 2018 The data demonstrated that low-dose arsenic trioxide (0.1 microM) enhanced the viability and apoptosis of tumor cells expressing hERG channels following long-term incubation. Arsenic Trioxide 36-52 ETS transcription factor ERG Homo sapiens 129-133 30127993-8 2018 Therefore, we hypothesized that this hormesis effect of low-dose arsenic trioxide on tumor cells may be associated with the hERG channel. Arsenic Trioxide 65-81 ETS transcription factor ERG Homo sapiens 124-128 30127993-9 2018 Furthermore, low dose arsenic trioxide promoted the hERG-channel current by changing the kinetics of channel gating and prolonging the open-channel stage. Arsenic Trioxide 22-38 ETS transcription factor ERG Homo sapiens 52-56 30127993-10 2018 Simultaneously, high-dose As2O3 (1 or 10 microM) significantly reduced the expression of hERG in tumor cells compared with the control group, which resulted in reduced proliferation rate and promotion of apoptotic rate. Arsenic Trioxide 26-31 ETS transcription factor ERG Homo sapiens 89-93 30127993-11 2018 The results of the present study demonstrate that the dual effects of arsenic trioxide on hERG channels vary according to concentration, resulting in the dual effects on tumor cells. Arsenic Trioxide 70-86 ETS transcription factor ERG Homo sapiens 90-94 30127993-12 2018 This provides a theoretical basis for the potential clinical application of arsenic trioxide, suggesting that hERG channels are an important target in preventing and treating tumorigenesis during arsenicosis. Arsenic Trioxide 76-92 ETS transcription factor ERG Homo sapiens 110-114 28521025-4 2017 In our study, we found a new pathway underlying As2O3-induced cardiotoxicity that As2O3 accelerates lysosomal degradation of hERG on plasma membrane after using brefeldin A (BFA) to block protein trafficking. Arsenic Trioxide 48-53 ETS transcription factor ERG Homo sapiens 125-129 28521025-4 2017 In our study, we found a new pathway underlying As2O3-induced cardiotoxicity that As2O3 accelerates lysosomal degradation of hERG on plasma membrane after using brefeldin A (BFA) to block protein trafficking. Arsenic Trioxide 82-87 ETS transcription factor ERG Homo sapiens 125-129 28521025-5 2017 Then we explored pharmacological rescue strategies on As2O3-induced LQTS, and found that 4 therapeutic agents exert rescue efficacy via 3 different pathways: fexofenadine and astemizole facilitate hERG trafficking via promotion of channel-chaperone formation after As2O3 incubation; ranolazine slows hERG degradation in the presence of As2O3; and resveratrol shows significant attenuation on calcium current increase triggered by As2O3. Arsenic Trioxide 54-59 ETS transcription factor ERG Homo sapiens 197-201 28521025-5 2017 Then we explored pharmacological rescue strategies on As2O3-induced LQTS, and found that 4 therapeutic agents exert rescue efficacy via 3 different pathways: fexofenadine and astemizole facilitate hERG trafficking via promotion of channel-chaperone formation after As2O3 incubation; ranolazine slows hERG degradation in the presence of As2O3; and resveratrol shows significant attenuation on calcium current increase triggered by As2O3. Arsenic Trioxide 54-59 ETS transcription factor ERG Homo sapiens 300-304